Category: Neurology

Brain MR in chronic fatigue syndrome

Abstract:

PURPOSE: To determine the prevalence of MR white matter abnormalities in patients with chronic fatigue syndrome (CFS).

METHODS: Brain MR studies of 43 patients (29 women and 14 men, 22 to 78 years old) with a clinical diagnosis of CFS (n = 15), CFS with associated depression (n = 14), and CFS with associated other psychiatric disorders, namely, anxiety and somatization disorder (n = 14), were compared with brain MR studies in 43 age- and sex-matched control subjects.

RESULTS: MR findings were abnormal in 13 (32%) of the patients in the study group (ages 34 to 78 years) and in 12 (28%) of the control subjects (ages 26 to 73 years). One patient with CFS had multiple areas of demyelination in the supratentorial periventricular white matter. Another patient with CFS and associated depression had a single focus of probable demyelination in the supratentorial periventricular white matter. In four patients with CFS (ages 34 to 48 years) MR abnormalities consisted of one or several punctate hyperintense foci in the corona radiata, centrum ovale, and frontal white matter. The remaining seven patients (ages 50 to 78 years) had frontoparietal subcortical white matter foci of high T2 signal. The prevalence of white matter hyperintensities was not different between the patients and the control subjects.

CONCLUSIONS: Our findings suggest that no MR pattern of white matter abnormalities is specific to CFS.

 

Source: Greco A, Tannock C, Brostoff J, Costa DC. Brain MR in chronic fatigue syndrome. AJNR Am J Neuroradiol. 1997 Aug;18(7):1265-9. http://www.ajnr.org/content/18/7/1265.long (Full article)

 

Increased brain serotonin function in men with chronic fatigue syndrome

Recent neuroendocrine studies suggest that patients with chronic fatigue syndrome may have increased brain serotonin activity.1 2 This could be relevant to the pathophysiology of chronic fatigue syndrome because serotonin pathways have a role in mediating central fatigue.3 Currently, however, the existence of abnormal serotonin neuroendocrine function in patients with chronic fatigue syndrome is controversial because of contradictory findings from samples of heterogeneous patients 4 5 and the use of serotonin probes such as buspirone, which are of doubtful pharmacological specificity.1 We aimed to measure the increase in plasma prolactin after administration of the selective serotonin releasing agent d-fenfluramine in men rigorously diagnosed as having the chronic fatigue syndrome and carefully matched healthy controls.

You can read the rest of this article here: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2127129/pdf/9251547.pdf

 

Source: Sharpe M, Hawton K, Clements A, Cowen PJ. Increased brain serotonin function in men with chronic fatigue syndrome. BMJ. 1997 Jul 19;315(7101):164-5. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2127129/

 

Does the chronic fatigue syndrome involve the autonomic nervous system?

Abstract:

PURPOSE: To investigate the role of the autonomic nervous system in the symptoms of patients with chronic fatigue syndrome (CFS) and delineate the pathogenesis of the orthostatic Intolerance and predisposition to neurally mediated syncope reported in this patient group.

PATIENTS AND METHODS: Twenty-three CFS patients and controls performed a battery of autonomic function tests. The CFS patients completed questionnaires pertaining to autonomic and CFS symptoms, their level of physical activity, and premorbid and coexisting psychiatric disorders. The relationship between autonomic test results, cardiovascular deconditioning, and psychiatric disorders was examined with multivariate statistics and the evidence that autonomic changes seen in CFS might be secondary to a postviral, idiopathic autonomic neuropathy was explored.

RESULTS: The CFS subjects had a significant increase in baseline (P < 0.01) and maximum heart rate (HR) on standing and tilting (both P < 0.0001). Tests of parasympathetic nervous system function (the expiratory inspiratory ratio, P < 0.005; maximum minus minimum HR difference, P < 0.05), were significantly less in the CFS group as were measures of sympathetic nervous system function (systolic blood pressure decrease with tilting, P < 0.01; diastolic blood pressure decrease with tilting, P < 0.05; and the systolic blood pressure decrease during phase II of a Valsalva maneuver, P < 0.05). Twenty-five percent of CFS subjects had a positive tilt table test. The physical activity index was a significant predictor of autonomic test results (resting, sitting, standing, and tilted HR, P < 0.05 to P < 0.009); and the blood pressure decrease in phase II of the Valvalsa maneuver, P < 0.05) whereas premorbid and coexistent psychiatric conditions were not. The onset of autonomic symptoms occurred within 4 weeks of a viral infection in 46% of patients-a temporal pattern that is consistent with a postviral, idiopathic autonomic neuropathy.

CONCLUSION: Patients with CFS show alterations in measures of sympathetic and parasympathetic nervous system function. These results, which provide the physiological basis for the orthostatic intolerance and other symptoms of autonomic function in this patient group, may be explained by cardiovascular deconditioning, a postviral idiopathic autonomic neuropathy, or both.

 

Source: Freeman R, Komaroff AL. Does the chronic fatigue syndrome involve the autonomic nervous system? Am J Med. 1997 Apr;102(4):357-64. http://www.ncbi.nlm.nih.gov/pubmed/9217617

 

Selective impairment of auditory processing in chronic fatigue syndrome: a comparison with multiple sclerosis and healthy controls

Abstract:

The most consistent deficit observed in individuals with Chronic Fatigue Syndrome has been in efficiency of information processing. To examine the possibility of a modality-specific impairment, the present study examined subjects with Chronic Fatigue Syndrome, multiple sclerosis, and healthy controls on an auditory-versus visual-paced serial-addition test. 20 subjects with Chronic Fatigue Syndrome, 20 subjects with clinically definite Multiple Sclerosis, and 20 sedentary healthy controls were compared.

One-half of the subjects in each group were administered the Paced Auditory Serial Addition Test and the other half were administered the Paced Visual Serial Addition Test. The group with Chronic Fatigue Syndrome was differentially impaired on the auditory relative to the visual processing task. The group with Multiple Sclerosis was equally impaired on both versions of the task. The results are discussed within the framework of Baddeley’s model of working memory.

 

Source: Johnson SK, DeLuca J, Diamond BJ, Natelson BH. Selective impairment of auditory processing in chronic fatigue syndrome: a comparison with multiple sclerosis and healthy controls. Percept Mot Skills. 1996 Aug;83(1):51-62. http://www.ncbi.nlm.nih.gov/pubmed/8873173

 

Multiple chemical sensitivity disorder in patients with neurotoxic illnesses

Abstract:

The data of 466 subjects suffering from neurologic disorders which are suggested to be caused by neurotoxic agents in their environment retrospectively was evaluated and documented. Among these cases there were 151 subjects with symptoms of Multiple Chemical Sensitivity Disorder (MCSD). The relationship between the neurological health impairments and neurotoxic agents in the environment of these patients was characterised using five different categories (probable = A, possible = B, uncertain = C, unclarified = D, not probable = E). From the 466 patients 320 subjects (69%) could be assigned to the categories A and B, respectively.

Within theses 320 cases with chronic neurotoxic health impairments 136 subjects (79 females and 57 males) showed signs of MCSD. Age and gender of cases as well as duration and character of exposure to neurotoxic substances retrospectively were assessed from the explicit files of the patients, which had been made anonymous for this purpose. Frequency of characteristic symptoms of neurotoxicity were analysed. Results are given for patients with neurotoxic health impairments with MCSD (n = 136) and without MCSD (n = 184).

Neurotoxic substances which were used as indoor wood preservatives (mainly Pentachlorophenol and/or Lindane) were found to be the causative agents in 63% of the cases with neurotoxic health impairments and MCSD. Other important neurotoxic substances to which the patients were mainly exposed were organic solvents (25%), formaldehyde (15%), dental materials (15%), pyrethroides (13%), and other biocides (19%) (multiple exposures were possible). The time of exposure was calculated as being > or = 10 years for 55% of the patients with MCSD and for 50% of the group with neurotoxic health impairments but without MCSD.

Out of the 184 cases with neurotoxic health impairments but without MCSD there were 22%, and out of the 136 cases with MCSD there were 39% who showed all symptoms of chronic fatigue syndrome. 53% of the cases with MCSD had an allergic disposition compared to only 20% of the cases without MCSD.

This work is not a controlled epidemiological study but a retrospective documentation and evaluation of data related to environmental medicine. With the present documentation in this purely descriptive manner the proof of a causal relationship was not possible or intended. But because corresponding epidemiological studies are lacking, this documentation can give important information on characteristic features of Multiple Chemical Sensitivity Disorder and chronic neurotoxic health impairments. Such information is essential for planning and carrying out epidemiological studies urgently needed in this field.

Comment in:

Comment on K. Lohmann, Anke Pröhl, E. Schwarz. Multiple chemical sensitivity in patients with neurotoxic illnesses. Gesundheitswesen. 1997 [Article in German]

 

Source: Lohmann K, Pröhl A, Schwarz E. Multiple chemical sensitivity disorder in patients with neurotoxic illnesses. Gesundheitswesen. 1996 Jun;58(6):322-31. [Article in German] http://www.ncbi.nlm.nih.gov/pubmed/8766847

 

Neuroimaging in chronic fatigue syndrome

The link between viral infection, the brain, and fatiguing illnesses has a long history. This combination forced itself on the medical imagination after events in Austria in the winter of 1916-17. A virulent form of influenza was noted, characteristically, to produce lethargy and later, to leave a host of neurological deficits in its wake. By the spring of 1918 several English cases of encephalitis lethargica had been reported and in the next year the disease was notifiable. The peak of the epidemic occurred in 1924 in the United Kingdom, at which time the Board of Control reported that many cases had been admitted to hospital with psychiatric disturbances.1 Hence the notion that apparent psychiatric illnesses may be misdiagnosed manifestations of a postinfectious cerebral disease began; it refuses to disappear.23

You can read the rest of this article here: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC486356/pdf/jnnpsyc00017-0001.pdf

 

Source: Cope H, David AS. Neuroimaging in chronic fatigue syndrome. J Neurol Neurosurg Psychiatry. 1996 May;60(5):471-3. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC486356/

 

Brainstem hypoperfusion in CFS

Comment on: Brainstem perfusion is impaired in chronic fatigue syndrome. [QJM. 1995]

 

Sir, Costa and his colleagues {QJ Med 1995; 88:767-73) are to be congratulated for providing more information about chronic fatigue syndrome. Hypocapnia is a powerful and readily available cerebral vasoconstrictor.1

The ‘cerebral vasoconstriction, and reduction in cerebral blood flow, are initiated when the arterial pCO2 has fallen 2 mmHg below normal. When the pCO2 has fallen by 25 mmHg, cerebral blood flow is decreased by about one third … the maximum possible reduction of blood flow that can be achieved by respiratory alkalaemia is of the order of 40 per cent’.2

You can read the rest of this comment here: http://qjmed.oxfordjournals.org/content/89/2/163.1.long

 

Source: Nixon PG. Brainstem hypoperfusion in CFS. QJM. 1996 Feb;89(2):163-4. http://qjmed.oxfordjournals.org/content/89/2/163.1.long

 

Comparison of 99m Tc HMPAO SPECT scan between chronic fatigue syndrome, major depression and healthy controls: an exploratory study of clinical correlates of regional cerebral blood flow

Abstract:

An explorative analysis of the relationship between symptomatology and cerebral blood flow in the chronic fatigue syndrome (CFS) as assessed with 99mTc HMPAO SPECT scan reveals statistically significant positive correlations between frontal blood flow on the one hand and objectively and subjectively assessed cognitive impairment, self-rating of physical activity limitations and total score on Hamilton Depression Rating Scale on the other. A pathophysiological role of frontal blood flow in the cognitive impairment and physical activity limitations in CFS is hypothesized.

A comparison of cerebral blood flow between CFS, major depression (MD) and healthy controls (HC) has been performed. A lower superofrontal perfusion index is demonstrated in MD as compared with both CFS and HC. There is neither a global nor a marked regional hypoperfusion in CFS compared with HC. Asymmetry (R > L) of tracer uptake at parietotemporal level is demonstrated in CFS as compared with MD.

 

Source: Fischler B, D’Haenen H, Cluydts R, Michiels V, Demets K, Bossuyt A, Kaufman L, De Meirleir K. Comparison of 99m Tc HMPAO SPECT scan between chronic fatigue syndrome, major depression and healthy controls: an exploratory study of clinical correlates of regional cerebral blood flow. Neuropsychobiology. 1996;34(4):175-83. http://www.ncbi.nlm.nih.gov/pubmed/9121617

 

Corticotropin releasing hormone in the pathophysiology of melancholic and atypical depression and in the mechanism of action of antidepressant drugs

Abstract:

Hypercortisolism in depression seems to preferentially reflect activation of hypothalamic CRH secretion. Although it has been postulated that this hypercortisolism is an epiphenomenon of the pain and stress of major depression, our data showing preferential participation of AVP in the hypercortisolism of chronic inflammatory disease suggest specificity for the pathophysiology of hypercortisolism in depression.

Our findings that imipramine causes a down-regulation of the HPA axis in experimental animals and healthy controls support an intrinsic role for CRH in the pathophysiology of melancholia and in the mechanism of action of psychotropic agents. Our data suggest that hypercortisolism is not the only form of HPA dysregulation in major depression.

In a series of studies, commencing in patients with Cushing’s disease, and extending to hyperimmune fatigue states such as chronic fatigue syndrome and examples of atypical depression such as seasonal affective disorder, we have advanced data suggesting hypofunction of hypothalamic CRH neurons. These data raise the question that the hyperphagia, hypersomnia, and fatigue associated with syndromes of atypical depression could reflect a central deficiency of a potent arousal-producing anorexogenic neuropeptide.

In the light of data presented elsewhere in this symposium regarding the role of a hypofunctioning hypothalamic CRH neuron in susceptibility to inflammatory disease, these data also raise the question of a common pathophysiological mechanism in syndromes associated both with inflammatory manifestations and atypical depressive symptoms. This concept of hypofunctioning of hypothalamic CRH neurons in these disorders also raises the question of novel forms of neuropharmacological intervention in both inflammatory diseases and atypical depressive syndromes.

 

Source: Gold PW, Licinio J, Wong ML, Chrousos GP. Corticotropin releasing hormone in the pathophysiology of melancholic and atypical depression and in the mechanism of action of antidepressant drugs. Ann N Y Acad Sci. 1995 Dec 29;771:716-29. http://www.ncbi.nlm.nih.gov/pubmed/8597444

 

Auditory brain stem evoked potentials in the evaluation of chronic fatigue syndrome

Abstract:

The Chronic Fatigue Syndrome (CFS) was formally defined to describe disabling fatigue of multifactorial ethology with depression and immunologic dysfunctions linked to some currently recognized infectious agents. In most cases neurophysiological tests reveal abnormalities.

In this paper the Authors use low (11 pps) and high (51-71 pps) frequency ABR to evaluate the electrophysiological function of auditory brainstem responses. Eighteen patients with suspected CFS, between the ages of 17 and 63, were examined. Eleven subjects had clinically diagnosed “true” CFS (CDC criteria modified by Fukuda). The 11 pps frequency test did not reveal a high number of abnormalities in the patients in question.

However, the high frequency stimulation test (with 51 and 71 pps) which was statistically significant (P = 0.009) revealed numerous aberrations in 7 patients; absence of the first wave in 1 case, in 5 numerous wave gap delays and in 1 patient absence of the first wave and numerous wave gap delays. The high frequency test did not show many abnormalities for the 4 remaining patients. For the 7 “non CFS” subjects, the clinical-audiological comparison showed no statistical significance (P = 0.920).

The Authors hypothesize that the absence of the first wave in the CFS Subject may well indicate a cyto-neural junction disease in the organ of Corti. The combined analysis of clinical and audiological data showed that the described tests are more reliable when employed in dealing with patients with clinically assessed “true” CFS.

 

Source: Bianchedi M, Croce A, Moretti A, Neri G, Barberio A, Iezzi A, Pizzigallo E. Auditory brain stem evoked potentials in the evaluation of chronic fatigue syndrome. Acta Otorhinolaryngol Ital. 1995 Dec;15(6):403-10. [Article in Italian] http://www.ncbi.nlm.nih.gov/pubmed/8711992